NASA Scientific and Technical Aerospace Reports

authorized. Additionally, the authors observed injury rate and potential injury risk factors. Fifteen infantrymen fired 15 shots
using a weapon system producing 59. 09 ft-lbs of recoil energy. Markers of injury assessed pre- firing, immediately post-firing,
and 24, 48, 72 and 96 hours post-firing included subjective pain, pain-pressure threshold, bruising, range of motion, strength,
a lifting task, and laboratory markers. Thermal imaging and MRI were used to assess skin temperature and edema. Data were
analyzed using repeated-measures ANOVA, Pearson correlations, and descriptive statistics. All 15 volunteers exhibited
bruising at the anterior shoulder, and 11 reported pain with motion post- firing. Fourteen volunteers (93%) sustained evidence
of soft tissue injury on MRI. Three (20%) sustained facial lacerations. Skin tissue temperature increased immediately
post-firing and returned to baseline 24 hours later. Dominant handgrip strength had the best predictive value for injury severity
on MRI. The authors conclude that soldiers are at risk for soft tissue contusions and lacerations at the upper threshold of
allowable recoil energy. Injury was characterized by elevated skin temperature, pain with motion, and decreased pain threshold
immediately post-firing. Signal intensity changes on MRI were consistent with muscle contusion for up to 96 hours post-firing.
(21 tables, 23 figures, 55 refs.)
DTIC
Injuries; Physiological Effects; Shoulders
20040111526 Texas Univ., Houston, TX
Radiation-Induced Chemosensitization: Potentiation of Antitumor Activity of Polymer-Drug Conjugates
Li, Chun; Apr. 2004; 34 pp.; In English
Contract(s)/Grant(s): DAMD17-00-1-0314
Report No.(s): AD-A425533; No Copyright; Avail: CASI; A03, Hardcopy
This study was aimed at evaluating the enhanced antitumor response to radiotherapy by poly(L-glutamic acid)- paclitaxel
(PG-TXL) conjugate. We compared the ability of paclitaxel and PG-TXL to sensitize radioresponse using both tumor growth
delay and tumor curability as the end points. Furthermore, the effect of treatment schedule on the radiosensitizing activity of
PG-TXL as well as the effect of PG-TXL on the sensitivity of normal tissues to radiation was also studied. Our data
demonstrate significant synergistic interaction between PG-TXL and tumor radiation. Compared to paclitaxel, PG-TXL
enhanced the response of tumors to radiation for approximately 4 folds. Importantly, the enhanced antitumor activity was
achieved without apparent effect on the normal tissues. Our results also suggest that PG-TXL may exert its radiosensitizing
effect through multiple mechanisms, one of which being sustained release of paclitaxel in the tumor from PG-TXL. This study
has lead to a National Cancer Institute-sponsored clinical study that has been initiated at the University of Texas M. D.
Anderson Cancer Center.
DTIC
Cancer; Chemotherapy; Conjugates; Conjugation; Drugs; Radiation Therapy
20040111527 Cold Spring Harbor Lab., New York, NY
Cloning of Tumor Suppressor Genes in Breast Cancer
Hamaguchi, Masaaki; May 2004; 17 pp.; In English
Contract(s)/Grant(s): DAMD17-00-1-0206
Report No.(s): AD-A425534; No Copyright; Avail: CASI; A03, Hardcopy
Breast cancer arises through the accumulation of genetic alterations that affect two classes of genes, ongogenes and tumor
suppressor genes. These genes must be identified for several reasons. Characterization of the genes that drive carcinogenesis
will facilitate a better understanding of cancer development. As part of this big picture, we have studied tumor suppressor
genes involved in breast cancer. A tumor suppressor candidate, DBC2 was analyzed. DBC2 is composed of a RAS domain,
protein-protein interacting domains, and DNA binding domain. DBC2 expression is extinguished by hypermethylation in more
than half of breast tumors we tested. When DBC2 expression was induced in tumor Cells, the cell growth was expressed.
Additionally, mutants we discovered in breast cancer specimens were found to lack the tumor suppressor function. We are
studying DBC2’s physiological roles by expression microarray analysis, protein- protein interaction studies, and functional
analysis. We have identified several genes upregulated by DBC2 and potential candidates for interaction. We have also
established techniques to control DBC2 expression, both induction and suppression, which will facilitate further analysis of
DBC2.
DTIC
Cancer; Cloning (Biology); Genetic Engineering; Mammary Glands; Tumor Suppressor Genes
166